RESPONSE OF RAT CEREBRAL SOMATOSTATINERGIC SYSTEM TO A HIGH AMMONIA DIET

It has been reported that ingestion of an ammonium-containing diet pro duces hyperammonemia without encephalopathy, thus permitting the study of the specific effects of ammonia toxicity. The present study invest igated the rat cerebral somatostatinergic system using this experiment al model of hyperammonemia. Wistar rats were fed a high ammonia diet p repared by mixing a standard diet with ammonium acetate (20% w/w); in addition, 5 mM of ammonium acetate was added to their water supply. Co ntrol rats were fed with a standard diet. The animals were sacrificed at 3, 7 and 15 days of ammonia ingestion. Ammonia levels in blood had increased approximate to 3-fold at 7 days of ammonia ingestion. These changes were associated with a significant decrease in the specific bi nding of somatostatin (SS) to putative receptors sites in the frontopa rietal cortex and hippocampus al 7 and 15 days after starting the high ammonia diet. Scatchard analysis shows that the decrease in SS bindin g resulted from a decrease in the number of available SS receptors rat her than a change in receptor affinity. No changes in the somatostatin -like immunoreactivity content (SSLI) were detected in either brain ar ea al the three study times. These results suggest that hyperammonemia alone can affect the rat brain somatostatinergic system. However, the animal model of hyperammonemia used here is insufficient to produce e ncephalopathy despite the significant increase in serum ammonia. Copyr ight (C) 1996 Elsevier Science Ltd